The purpose of this research project is to attempt to better understand the pathogenetic role of rheumatoid factor and complement in the inflammatory process producing tissue damage in rheumatoid arthritis. The tissues most subject to involvement by this inflammatory process in rheumatoid arthritis are the synovial tissue linning diarthroidal joints with subsequent destruction of the joint and bone in proximity to it; the vascular tissue, especially small vessels such as arterioles and venules; and finally, the parenchymal tissue of the heart and lung. The mechanism of tissue injury, as it is presently understood, occurs by means of immune complex deposition (formed by autologous IgG and rheumatoid factor which is an anti-gamma globulin) in the various tissues mentioned. Complement is then fixed to the immune complexes and, in turn, produces an intense inflammatory reaction involving neutrophiles leading to tissue damage. This project attempts to assess the relationship of the complement fixing capacity (measured by quantitative assay) of polyclonal rheumatoid factors to disease course and response to therapy in several patients with RA and the same individual patients at different times. A quantitative assay measuring complement fixation by rheumatoid factor using sheep erythrocytes coated with reduced and alkylated rabbit IgG hemolysin as the target cell will be employed.